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中国精品科技期刊2020
刘雪城,金皓洁,陈彬辉,等. 蚕豆苗提取物对帕金森病的保护作用[J]. 食品工业科技,2022,43(22):379−386. doi: 10.13386/j.issn1002-0306.2022010053.
引用本文: 刘雪城,金皓洁,陈彬辉,等. 蚕豆苗提取物对帕金森病的保护作用[J]. 食品工业科技,2022,43(22):379−386. doi: 10.13386/j.issn1002-0306.2022010053.
LIU Xuecheng, JIN Haojie, CHEN Binhui, et al. Protective Effect of Broad Bean Seedling Extract on Parkinson's Disease[J]. Science and Technology of Food Industry, 2022, 43(22): 379−386. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2022010053.
Citation: LIU Xuecheng, JIN Haojie, CHEN Binhui, et al. Protective Effect of Broad Bean Seedling Extract on Parkinson's Disease[J]. Science and Technology of Food Industry, 2022, 43(22): 379−386. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2022010053.

蚕豆苗提取物对帕金森病的保护作用

Protective Effect of Broad Bean Seedling Extract on Parkinson's Disease

  • 摘要: 目的:研究蚕豆苗提取物(Broad bean seedling extract,BSE)抗帕金森病的作用及初步机制。方法:采用50 μmol/L六羟基多巴胺(6-Hydroxydopamine,6-OHDA)诱导PC-12、SH-SY5Y细胞损伤,应用MTT法检测不同浓度BSE对神经细胞增殖的影响,并测定神经细胞中活性氧(Reactive oxygen species,ROS)水平、线粒体膜电位以及细胞凋亡情况。采用腹腔注射1-甲基-4-苯基-1,2,3,6-四氢吡啶(1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine,MPTP)建立帕金森病小鼠模型,设置空白对照组、模型对照组、500 mg/kg BSE组、300 mg/kg BSE组、25 mg/kg左旋多巴组,每组6只。通过爬杆试验、转轴实验和抓力实验观察BSE对小鼠行为学功能的影响,并测定BSE对小鼠脑组织中丙二醛(Malondialdehyde,MDA)、超氧化物歧化酶(Superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(Glutathione peroxidase,GSH-Px)含量的影响。结果:PC-12和SH-SY5Y细胞经6-OHDA诱导后,细胞增殖受到抑制、细胞活性氧水平上升、线粒体膜电位下降,细胞凋亡增多。BSE预处理可极显著降低神经细胞的细胞增殖抑制率、活性氧水平,增加线粒体膜电位,并抑制细胞凋亡(P<0.01)。BSE可极显著缩短MPTP帕金森病模型小鼠的爬杆时间,增加抓力和延长转轴时间,提高小鼠脑组织SOD和GSH-Px水平,降低MDA含量,并抑制脑组织脂质过氧化(P<0.01)。结论:BSE对神经细胞具有保护作用,能明显改善帕金森病模型小鼠的症状,提示BSE可能对帕金森病具有潜在的治疗意义。

     

    Abstract: Objective: To study the protective effect of broad bean seedling extract (BSE) on Parkinson’s disease. Methods: PC-12 and SH-SY5Y cell injury were induced by 50 μmol/L 6-OHDA. The effects of BSE on the proliferation of neuro cells were determined by MTT method. The effects of BSE on reactive oxygen species (ROS), mitochondrial membrane potential and apoptosis in neuro cells were measured. The mouse model of Parkinson’s disease was established by intraperitoneal injection of MPTP, and the mice were divided into blank control group, model control group, 500 mg/kg BSE group, 300 mg/kg BSE group and 25 mg/kg L-dopa group with 6 rats in each group. The effects of BSE on the behavioral function of mice were studied via pole climbing test, rotation test and grip test, and the effects of BSE on the contents of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the brain of mice were determined by the test kit. Results: After PC-12 and SH-SY5Y neuro cells were treated by 6-OHDA, the cell proliferation was inhibited, the level of reactive oxygen species increased, the mitochondrial membrane potential decreased and the apoptosis increased. After pretreatment with BSE, the inhibition rate of cell proliferation and the level of reactive oxygen species were significantly decreased, the mitochondrial membrane potential was increased and the apoptosis was inhibited (P<0.01). BSE could significantly shorten the rod climbing time, increase the grip and prolong the rotation time, increase the levels of SOD and GSH-Px in brain tissue, decrease the content of MDA and inhibit lipid peroxidation in brain tissue of MPTP Parkinson’s disease model mice (P<0.01). Conclusion: BSE had a protective effect on nerve cells and can significantly improve the symptoms of Parkinson’s disease in mice. These results suggested that BSE might have potential therapeutic significance for Parkinson’s disease.

     

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